Evidence map›Paper›PMID 29589276›Full record

ArticleNeurotoxicity research2018

Dipentylammonium Binds to the Sigma-1 Receptor and Protects Against Glutamate Toxicity, Attenuates Dopamine Toxicity and Potentiates Neurite Outgrowth in Various Cultured Cell Lines.

James M Brimson, Stephen T Safrany, Heider Qassam, Tewin Tencomnao

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  6. Article
  7. Sigma 1 Receptor and Its Pivotal Role in Neurological Disorders.ACS pharmacology & translational science · 2025
    Review
  8. Review
  9. Review
  10. Sphingoid Bases Regulate the Sigma-1 Receptor-Sphingosine andInternational journal of molecular sciences · 2023
    Article
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  16. Article
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  18. Article
  19. Hazards of UsingFrontiers in pharmacology · 2020
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 3 countries.

James M BrimsonAge-related Inflammation and Degeneration Research Unit, Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10230, Thailand.
Stephen T SafranyRoyal College of Surgeons in Ireland, Medical University of Bahrain, P.O. Box 15503, Adliya, Bahrain.
Heider QassamDepartment of Molecular and Cell Biology, University in Leicester, Henry Wellcome Building, Lancaster Road, Leicester, LE1 7RH, UK.
Tewin TencomnaoAge-related Inflammation and Degeneration Research Unit, Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10230, Thailand. Tewintecomnao@gmail.com.
Chulalongkorn University · THRoyal College of Surgeons in Ireland - Bahrain · BHUniversity of Leicester · GB

Funding

The National Research University Project, Office of Higher Education Commission. NRU-59-057-AS
6 · The paper itself

Abstract

Alzheimer's disease is a neurodegenerative disease that affects 44 million people worldwide, costing the world $605 billion to care for those affected not taking into account the physical and psychological costs for those who care for Alzheimer's patients. Dipentylammonium is a simple amine, which is structurally similar to a number of other identified sigma-1 receptor ligands with high affinities such as (2R-trans)-2butyl-5-heptylpyrrolidine, stearylamine and dodecylamine. This study investigates whether dipentylammonium is able to provide neuroprotective effects similar to those of sigma-1 receptor agonists such as PRE-084. Here we identify dipentylammonium as a sigma-1 receptor ligand with nanomolar affinity. We have found that micromolar concentrations of dipentylammonium protect from glutamate toxicity and prevent NFκB activation in HT-22 cells. Micromolar concentrations of dipentylammonium also protect stably expressing amyloid precursor protein Swedish mutant (APP/Swe) Neuro2A cells from toxicity induced by 150 μM dopamine, suggesting that dipentylammonium may be useful for the treatment of Parkinsonian symptoms in Alzheimer's patients which are often associated with a more rapid deterioration of cognitive and physical ability. Finally, we found that low micromolar concentrations of dipentylammonium could out preform known sigma-1 receptor agonist PRE-084 in potentiating neurite outgrowth in Neuro2A cells, further suggesting that dipentylammonium has a potential use in the treatment of neurodegenerative diseases and could be acting through the sigma-1 receptor.

Indexed as

AnimalsBoronic AcidsCell LineDopamineDose-Response Relationship, DrugExcitatory Amino Acid AgonistsGlutamic AcidHumansImidazolesL-Lactate DehydrogenaseNeuroblastomaNeuronal OutgrowthNeuroprotective AgentsNF-kappa BPentazocineProtein Transport4-(4,5-diphenyl-1H-imidazol-2-yl)phenylboronic acidBoronic AcidsDopamineExcitatory Amino Acid AgonistsGlutamic AcidImidazolesL-Lactate DehydrogenaseNeuroprotective AgentsNF-kappa BPentazocineReceptors, sigmaSigma-1 ReceptorTritiumAlzheimer’s diseaseNeuroprotectionNeurotoxicityParkinson’s diseaseSigma-1 receptor

Identifiers

PMID29589276
OpenAlexW2794663024

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.